Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Selenium (Se) is an essential trace-element that becomes toxic when present at high concentrations. Little is known regarding Se effects on parameters such as oxidative stress biomarkers. The aim of the present study was to investigate the effects of acute selenium exposure on oxidative stress biomarkers in a model organism, zebrafish (Danio rerio). Fish were exposed to selenium selenite at 1mgL(-1). Reduced glutathione (GSH), and metallothionein (MT) concentrations were determined in liver, kidney and brain, with MT also being determined in bile. Essential metals and trace-elements were also determined by inductively coupled mass spectrometry (ICP-MS) in order to verify possible metal homeostasis alterations. GSH concentrations in liver, kidney and brain increased significantly (1.05±0.03μmolg(-1) ww, 1.42±0.03μmolg(-1) ww and 1.64±0.03μmolg(-1) ww, respectively) in the Se-exposed group when compared to the controls (0.88±0.05μmolg(-1) ww, 0.80±0.04μmolg(-1) ww and 0.89±0.03μmolg(-1) ww for liver, kidney and brain, respectively). MT levels in Se-exposed liver (0.52±0.03μmolg(-1) ww) decreased significantly in comparison to the control group (0.64±0.02μmolg(-1) ww), while levels in bile increased, albeit non-significantly. This is in accordance with previous studies that indicate efficient biliary MT action, leading to a rapid metabolism and elimination of contaminants from the body. Levels in the brain increased significantly after Se-exposure (0.57±0.01μmolg(-1) ww) when compared to the control group (0.35±0.03μmolg(-1) ww) since this organ does not present a detoxification route as quick as the liver-gallbladder route. Several metal and trace-elements were altered with Se-exposure, indicating that excess of selenium results in metal dyshomeostasis. This is the first report on metal dyshomeostasis due to Se-exposure, which may be the first step in the mechanism of action of selenium toxicity, as is postulated to occur in certain major human pathophysiologies.
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http://dx.doi.org/10.1016/j.jtemb.2015.09.001 | DOI Listing |
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